SOCS3 expression correlates with severity of inflammation in mouse hepatitis virus strain 3-induced acute liver failure and HBV-ACLF.
10.1007/s11596-014-1281-5
- Author:
Yong LI
1
;
Mei-fang HAN
;
Wei-na LI
;
Ai-chao SHI
;
Yuan-ya ZHANG
;
Hong-yan WANG
;
Fa-xi WANG
;
Lan LI
;
Ting WU
;
Lin DING
;
Tao CHEN
;
Wei-ming YAN
;
Xiao-ping LUO
;
Qin NING
Author Information
1. Department and Institute of Infectious Diseases, University of Science and Technology, Wuhan, 430030, China, vamos_yong@hotmail.com.
- Publication Type:Journal Article
- MeSH:
Adult;
Alanine Transaminase;
blood;
Animals;
Aspartate Aminotransferases;
blood;
Blotting, Western;
End Stage Liver Disease;
genetics;
pathology;
virology;
Female;
Gene Expression;
Hepatitis, Viral, Animal;
genetics;
pathology;
virology;
Host-Pathogen Interactions;
Humans;
Interleukin-1beta;
genetics;
metabolism;
Interleukin-6;
genetics;
metabolism;
Leukocytes, Mononuclear;
metabolism;
virology;
Liver Failure, Acute;
genetics;
pathology;
virology;
Male;
Mice, Inbred BALB C;
Middle Aged;
Murine hepatitis virus;
physiology;
Reverse Transcriptase Polymerase Chain Reaction;
Severity of Illness Index;
Suppressor of Cytokine Signaling 3 Protein;
Suppressor of Cytokine Signaling Proteins;
blood;
genetics;
metabolism;
Tumor Necrosis Factor-alpha;
genetics;
metabolism;
Young Adult
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(3):348-353
- CountryChina
- Language:English
-
Abstract:
Recently, suppressor of cytokine signaling-3 (SOCS3) has been shown to be an inducible endogenous negative regulator of Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway which is relevant in inflammatory response, while its functions in acute liver failure and HBV-induced acute-on-chronic liver failure (HBV-ACLF) have not been fully elucidated. In this study, we explored the role of SOCS3 in the development of mouse hepatitis virus strain 3 (MHV-3)-induced acute liver failure and its expression in liver and peripheral blood mononuclear cells (PBMCs) of patients with HBV-ACLF. Inflammation-related gene expression was detected by real-time PCR, immunohistochemistry and Western blotting. The correlation between SOCS3 level and liver injury was studied. Our results showed that the SOCS3 expression was significantly elevated in both the liver tissue and PBMCs from patients with HBV-ACLF compared to mild chronic hepatitis B (CHB). Moreover, a time course study showed that SOCS3 level was increased remarkably in the liver of BALB/cJ mice at 72 h post-infection. Pro-inflammatory cytokines, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, were also increased significantly at 72 h post-infection. There was a close correlation between hepatic SOCS3 level and IL-6, and the severity of liver injury defined by alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, respectively. These data suggested that SOCS3 may play a pivotal role in the pathogenesis of MHV-3-induced acute liver failure and HBV-ACLF.
